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may be accompanied by mild dilatation of the ventricular system or (rarely) nodular meningeal
enhancement on post contrast images. Dilated perivascular Virchow-Robin spaces filled with
fungi result in the formation of nonenhancing cystic lesions of low density on CT scan, or low
signal intensity onT1-weighted MR images, and high signal intensity onT2-weighted MR
images. A mass effect from a “cryptococcoma” is rare and may be seen in ependyma or choroid
plexus.[738,752,759,765]
Cerebrospinal fluid (CSF) examination is most helpful for diagnosis of cryptococcal
meningitis by latex agglutination test for the antigen. Antigen may also be detected in serum.
The India ink preparation is usually positive. Typical CSF findings include a mildly elevated
protein, normal or slightly low glucose, and a lymphocytic pleocytosis. White blood cells and
red blood cells may not be numerous in the CSF in patients with AIDS because of the poor
inflammatory response to cryptococci. However, changes in serum titers of cryptococcal antigen
during treatment for acute meningitis or during suppressive therapy do not correlate with
outcome of therapy.[452,780]
Gross pathologic involvement of meninges is difficult to detect due to paucity of
inflammation. Involvement of brain parenchyma most often occurs in basal ganglia, midbrain,
and cerebellum. Small gelatinous pseudocysts may often be found in the region of the Virchow-
Robin spaces and superficial neocortex. Larger cysts may occur in basal ganglia and thalamus.
Microscopically, numerous poorly encapsulated organisms are found in lesions with minimal
inflammatory infiltrate of lymphocytes and plasma cells.[781]
The C neoformans organisms may be poorly encapsulated, and they are usually
accompanied by a sparse inflammatory reaction with only a few lymphocytes or macrophages.
Thus, a grossly apparent gelatinous exudate may not be present, though the patient may have
clinical signs and symptoms of meningitis. A methenamine silver stain may be necessary to
identify the organisms clearly in tissues.
For patients with CD4 lymphocytes counts <100/µL, prophylaxis with fluconazole or
ketoconazole may be useful. Fluconazole is most often used for secondary prophylaxis, since
many patients with treated C neoformans infections will have a recurrence without continued
suppressive therapy. Treatment with amphotericin B, flucytosine, and triazoles (fluconazole,
itraconazole) can be effective, though up to 30% of cases fail to respond to therapy.[208,396]
For acute infections, intravenous amphotericin B followed by oral fluconazole has shown
effectiveness. In some cases, institution of antiretroviral therapy has resulted in immune
reconstitution with exuberant inflammation around established foci of infection and onset of
more severe symptoms.[452]

MALIGNANT LYMPHOMA.-- Most CNS non-Hodgkin lymphomas seen with AIDS
are primary neoplasms. CNS involvement by systemic lymphomas is more often meningeal.
Overall, about 10% of patients with AIDS have CNS lymphoma at autopsy.[758] CNS
lymphomas are of the diffuse large cell variety, high grade, and of B-lymphocyte origin. They
are essentially an expansion of EBV-infected B-lymphocytes.[567] Patients may present with
non-localizing symptoms which include confusion, lethargy, and memory loss. Less frequent
findings include hemiparesis, aphasia, seizures, cranial nerve palsies, and headache.
Primary CNS lymphomas may be diagnosed clinically by radiographic findings. By
computed tomographic (CT) scans, the single or multiple lesions are hyperdense with solid or
ring enhancement. When they appear as multiple discrete ring-enhancing lesions, they are very
similar to those seen with toxoplasmosis. CT scans may show the distribution of the lesions to